Lesson 2 Crisan & Goldberg 2025 Ex

Environmental Biotechnology

🌱 What is Stenotrophomonas maltophilia complex (Smc)?

  • A group of Gram-negative Gammaproteobacteria (order Lysobacterales).
  • Found everywhere: soil, water, plants 🌿💧, but also in hospitals (ICUs, equipment, catheters) 🏥.
  • Very diverse: classified into 23 lineages.
    • Sm6 = S. maltophilia sensu stricto, the main one (includes famous strain K279a).
    • Sm1–Sm5, Sm7–Sm18 = sensu lato (closely related).
    • Sgn1–4 = distant cousins.
  • Multiple lineages infect humans (Sm2, Sm4a/b, Sm6, Sm13), while others mostly stay environmental.

💉 Why is Smc clinically important?

  • Opportunistic pathogen → can infect lungs, brain, skin, urinary tract, eyes, and blood.
  • Nosocomial menace: colonizes hospital equipment → blood infections can kill >65% of patients 😱.
  • High risk for CF, COPD, COVID-19, cancer patients.
  • In COVID-19 patients, Smc had highest multidrug resistance rates.
  • Risk factors: ventilators, catheters, tracheotomies, heavy antibiotic use.
  • Debate: is it always a pathogen or sometimes just a marker of severe illness?
  • Infections are rising 📈, due to:
    • More ICU admissions + cancer cases.
    • Better detection and recognition by clinicians.

🧩 How does Smc cause trouble?

Surface adhesion & biofilms

  • Forms biofilms (sticky communities of bacteria + polysaccharides, DNA, proteins) 🧽.
  • Uses flagella (tails) for movement + adhesion.
  • Fimbriae (tiny hair-like projections) help it stick.

Secreted weapons

  • Type II Secretion System (T2SS) → releases proteases like:
    • StmPr1: damages host junctions, kills cells, triggers IL-8 inflammation 🚨.
    • StmPr2/3: toxic, degrade proteins.
  • Type IV Secretion System (T4SS) → nanomachine that:
    • Kills macrophages, tweaks apoptosis in host cells.
    • Can also inject antibacterial toxins into other bacteria.
  • Iron uptake: produces siderophores to steal iron 🧲 (needed for metabolism).
  • Antibiotic resistance arsenal:
    • Efflux pumps export drugs (fluoroquinolones, tetracyclines, trimethoprim, sulfa).
    • β-lactamases (blaL1, blaL2) inactivate carbapenems.
    • Resistance gene distribution differs between lineages.
  • Diffusible signal factor (DSF) = a communication molecule that:
    • Boosts virulence, biofilm, siderophores.
    • Activates β-lactamase production → more antibiotic resistance.

🤝 How does Smc interact with others?

With bacteria

  • Found in mixed infections (with Pseudomonas aeruginosa, Staph aureus, E. coli).
  • Can be cooperative:
    • P. aeruginosa helps Smc colonize lungs.
  • Can be antagonistic:
    • Smc’s T4SS kills E. coli and P. aeruginosa.
    • Some lineages (e.g., STEN00241) use Type VI Secretion System (T6SS) = a harpoon gun 🎯 to kill competitors like Burkholderia.
    • Contact-Dependent Inhibition (CDI) systems: secreted “stick proteins” deliver toxins only to related strains.

With fungi 🍄

  • Fights Candida albicans and Aspergillus fumigatus: hinders growth, thickens fungal cell walls.

With viruses 🦠

  • Infected by bacteriophages (phages).
  • Hosts both lysogenic (integrate DNA) and lytic (kill bacteria) phages.
  • Smc genomes carry antiphage defense systems → shows phage battles are common.

🧭 Conclusions & Future Directions

  • Smc = emerging, multidrug-resistant global pathogen.
  • Equipped with:
    • Biofilms, secretion systems, efflux pumps, communication molecules.
    • Competitive interactions with bacteria, fungi, and phages.
  • Future research needs to focus on:
    • How virulence and resistance genes are regulated.
    • How other microbes influence Smc’s pathogenicity.
    • Exploring phages as therapy against resistant infections. 🚀

Quiz

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